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2. Phenotypic assays and sequencing are less sensitive than point mutation assays for detection of resistance in mixed HIV-1 genotypic populations

Author

Van Laethem, K., Van Vaerenbergh, K., Schmit, J.-C., Sprecher, S., Hermans, P., De Vroey, V., Schuurman, R., Harrer, T., Witvrouw, M., Van Wijngaerden, E., Stuyver, L., Van Ranst, M., Desmyter, J., De Clercq, E., and Vandamme, A.-M.

Subjects
Drug resistance in microorganisms -- Identification and classification, HIV (Viruses) -- Genetic aspects, Health
Abstract

The 151 and 215 amplification refractory mutation system (ARMS) is more accurate than other tests in detecting drug resistance in the virus that causes AIDS. ARMS was compared with T7 sequencing, cycle sequencing, the line probe assay (LiPA) HIV-1 RT test, and the recombinant virus assay (RVA).

Published
1999

5. Baseline HIV-1 genotypic resistance to a newly added nucleoside analogue is predictive for virologic failure of the change of therapy

Author

Van Vaerenbergh, K., Van Laethem, K., Van Wijngaerden, E., Schmit, J.c., Schneider, F., Ruiz, L., Clotet, B., Verhofstede, C., Van Wanzeele, F., Muyldermans, Gaetan, Simons, P., Stuyver, L., Hermans, Philip, Evans, C., De Clercq, Ellen, Desmyter, J., Vandamme, A.m., Surgery Specializations, Internal Medicine, and Vrije Universiteit Brussel

Published
2000

6. Cross-Resistance Profile Determination of Two Second-Generation HIV-1 Integrase Inhibitors Using a Panel of Recombinant Viruses Derived from Raltegravir-Treated Clinical Isolates

Author

Van Wesenbeeck, L., primary, Rondelez, E., additional, Feyaerts, M., additional, Verheyen, A., additional, Van der Borght, K., additional, Smits, V., additional, Cleybergh, C., additional, De Wolf, H., additional, Van Baelen, K., additional, and Stuyver, L. J., additional

Published
2011
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7. A PROPOSED SYSTEM FOR THE NOMENCLATURE OF HEPATITIS-C VIRAL GENOTYPES

Author

SIMMONDS, P ALBERTI, A ALTER, HJ BONINO, F BRADLEY, DW and BRECHOT, C BROUWER, JT CHAN, SW CHAYAMA, K CHEN, DS and CHOO, QL COLOMBO, M CUYPERS, HTM DATE, T DUSHEIKO, GM ESTEBAN, JI FAY, O HADZIYANNIS, SJ HAN, J and HATZAKIS, A HOLMES, EC HOTTA, H HOUGHTON, M IRVINE, B and KOHARA, M KOLBERG, JA KUO, G LAU, JYN LELIE, PN and MAERTENS, G MCOMISH, F MIYAMURA, T MIZOKAMI, M NOMOTO, A and PRINCE, AM REESINK, HW RICE, C ROGGENDORF, M SCHALM, SW SHIKATA, T SHIMOTOHNO, K STUYVER, L TREPO, C and WEINER, A YAP, PL URDEA, MS

Published
1994

8. Comparison of phenotypic and genotypic tropism determination in triple-class-experienced HIV patients eligible for maraviroc treatment

Author

Vandekerckhove, L., primary, Verhofstede, C., additional, Demecheleer, E., additional, De Wit, S., additional, Florence, E., additional, Fransen, K., additional, Moutschen, M., additional, Mostmans, W., additional, Kabeya, K., additional, Mackie, N., additional, Plum, J., additional, Vaira, D., additional, Van Baelen, K., additional, Vandenbroucke, I., additional, Van Eygen, V., additional, Van Marck, H., additional, Vogelaers, D., additional, Geretti, A. M., additional, and Stuyver, L. J., additional

Published
2010
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10. 5',9-Anhydro-3-(β-D-ribofuranosyl)purine nucleoside analogues as potential anti-HCV agents

Author

Chun, B.-K., primary, Clark, J. L., additional, Du, J., additional, Furman, P. A., additional, Hassan, A. E., additional, Hollecker, L., additional, McBrayer, T., additional, Otto, M. E., additional, Pankiewicz, K. W., additional, Patterson, S. E., additional, Rachakonda, S., additional, Schinazi, R. F., additional, Stuyver, L. J., additional, Wang, P. W., additional, Watanabe, K. A., additional, and Whitaker, T., additional

Published
2005
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12. Prevalence of Genotypic Resistance among Antiretroviral Drug-Naive HIV-1-Infected Patients in Belgium

Author

Van Vaerenbergh, K, primary, Debaisieux, L, additional, De Cabooter, N, additional, Declercq, C, additional, Desmet, K, additional, Fransen, K, additional, Maes, B, additional, Marissens, D, additional, Miller, K, additional, Muyldermans, G, additional, Sprecher, S, additional, Stuyver, L, additional, Vaira, D, additional, Verhofstede, C, additional, Zissis, G, additional, Van Ranst, M, additional, De Clercq, E, additional, Desmyter, J, additional, and Vandamme, A-M, additional

Published
2001
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13. Rapid genotyping of hepatitis C virus RNA-isolates obtained from patients residing in Western Europe

Author

Kleter, G.E.M. (Bernhard), Doorn, L.-J. (Leen-Jan) van, Stuyver, L. (L.), Maertens, G. (G.), Brouwer, J.T. (Johannes), Schalm, S.W. (Solko), Heijtink, R.A. (Rudolf), Quint, W.G.V. (Wim), Kleter, G.E.M. (Bernhard), Doorn, L.-J. (Leen-Jan) van, Stuyver, L. (L.), Maertens, G. (G.), Brouwer, J.T. (Johannes), Schalm, S.W. (Solko), Heijtink, R.A. (Rudolf), and Quint, W.G.V. (Wim)

Abstract

Two rapid genotyping methods for hepatitis C virus (HCV), the line probe assay (Inno‐LiPA) and the subtype‐specific core amplification system [Okamoto et al., (1992b) Journal of General Virology 73:673‐679], were applied to 58 HCV isolates which were typed as type 1 (n=37) and type 2 (n=21) by sequence analysis of the 5′ untranslated region (5′UTR). The line probe assay targets the 5′UTR and recognized 12 subtype 1a, 25 subtype 1b, 18 subtype 2a, 2 subtype 2b and 1 subtype 2d in accordance with sequence analysis of this region. Subtype‐specific core amplification revealed 7 discrepancies among the 37 type 1 isolates when compared to LiPA. A different subtype was observed in 3 isolates (la versus 1b), 2 isolates remained untyped and 2 isolates showed a coinfection of subtype la and 1b. The first 5 discrepancies were confirmed by sequence analysis of the core region whereas the coinfection could not be confirmed. Of the 21 type 2 isolates only one could be typed by subtype‐specific core amplification. HCV RNA was detected in all 21 cases after the general first round of polymerase chain reaction (PCR). Direct sequencing of the core region indicated sequence variation as a source of failure. It is concluded that LiPA results are conclusive for typing of HCV. However, LiPA is hampered occasionally for subtyping by lack o

Published
1995
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14. Baseline HIV Type 1 Genotypic Resistance to a Newly Added Nucleoside Analog Is Predictive of Virologic Failure of the New Therapy

Author

Vaerenbergh, K. Van, primary, Laethem, K. Van, additional, Wijngaerden, E. Van, additional, Schmit, J.-C., additional, Schneider, F., additional, Ruiz, L., additional, Clotet, B., additional, Verhofstede, C., additional, Wanzeele, F. Van, additional, Uyldermans, G. M, additional, Simons, P., additional, Stuyver, L., additional, Hermans, P., additional, Evans, C., additional, Clercq, E. De, additional, Desmyter, J., additional, and Vandamme, A.-M., additional

Published
2000
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22. Reply

Author

Pawlotsky, J.-M., primary, Stuyver, L., additional, and Dhumeaux, D., additional

Published
1996
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34. Study of genotypic and phenotypic HIV-1 dynamics of integrase mutations during raltegravir treatment: a refined analysis by ultra-deep 454 pyrosequencing.

Author

Armenia D, Vandenbroucke I, Fabeni L, Van Marck H, Cento V, D'Arrigo R, Van Wesenbeeck L, Scopelliti F, Micheli V, Bruzzone B, Lo Caputo S, Aerssens J, Rizzardini G, Tozzi V, Narciso P, Antinori A, Stuyver L, Perno CF, Ceccherini-Silberstein F, and Armenia, Daniele

Subjects
DOCUMENTATION, DRUG resistance in microorganisms, BIOLOGICAL evolution, HETEROCYCLIC compounds, HIV, HIV infections, MICROBIAL sensitivity tests, GENETIC mutation, PROTEINS, PHENOTYPES, SALVAGE therapy, ANTI-HIV agents, SEQUENCE analysis, GENOTYPES
Abstract

Background: The dynamics of raltegravir-resistant variants and their impact on virologic response in 23 HIV-1-infected patients, who started a salvage raltegravir-containing regimen, were investigated.Methods: Integrase population sequencing and Ultra-Deep-454 Pyrosequencing (UDPS) were performed on plasma samples at baseline and at raltegravir failure. All integrase mutations detected at a frequency ≥1% were considered to be reliable for the UDPS analyses. Phylogenetic and phenotypic resistance analyses were also performed.Results: At baseline, primary resistance mutations were not detected by both population and UDPS genotypic assays; few secondary mutations (T97A-V151I-G163R) were rarely detected and did not show any statistically association either with virologic response at 24-weeks or with the development of resistant variants at failure. At UDPS, not all resistant variants appearing early during treatment evolved as major populations during failure; only specific resistance pathways (Y143R-Q148H/R-N155H) associated with an increased rate of fitness and phenotypic resistance were selected.Conclusions: Resistance to raltegravir in integrase strand transfer inhibitor-naive patients remains today a rare event, which might be changed by future extensive use of such drugs. In our study, pathways of resistance at failure were not predicted by baseline mutations, suggesting that evolution plus stochastic selection plays a major role in the appearance of integrase-resistance mutations, whereas fitness and resistance are dominant factors acting for the late selection of resistant quasispecies. [ABSTRACT FROM AUTHOR]

Published
2012
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36. Cross-Resistance Profile Determination of Two Second-Generation HIV-1 Integrase Inhibitors Using a Panel of Recombinant Viruses Derived from Raltegravir-Treated Clinical Isolates

Author

Van Wesenbeeck, L., Rondelez, E., Feyaerts, M., Verheyen, A., Van der Borght, K., Smits, V., Cleybergh, C., De Wolf, H., Van Baelen, K., and Stuyver, L. J.

Abstract

ABSTRACTThe integrase inhibitor raltegravir (RAL) is currently used for the treatment of both treatment-naïve and treatment-experienced HIV-1-infected patients. Elvitegravir (EVG) is in late phases of clinical development. Since significant cross-resistance between RAL and EVG is observed, there is a need for second-generation integrase inhibitors (INIs) with a higher genetic barrier and limited cross-resistance to RAL/EVG. A panel of HIV-1 integrase recombinants, derived from plasma samples from raltegravir-treated patients (baseline and follow-up samples), were used to study the cross-resistance profile of two second-generation integrase inhibitors, MK-2048 and compound G. Samples with Q148H/R mutations had elevated fold change values with all compounds tested. Although samples with the Y143R/C mutation had reduced susceptibility to RAL, they remained susceptible to MK-2048 and compound G. Samples with the N155H mutation had no reduced susceptibility to compound G. In conclusion, our results allowed ranking of the INIs on the basis of the antiviral activities using recombinant virus stocks from RAL-treated patient viruses. The order according to decreasing susceptibility is compound G, MK-2048, and EVG.

Published
2010
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37. Synthesis and Structure−Activity Relationships of Novel Anti-hepatitis C Agents: N<SUP>3</SUP>,5‘-Cyclo-4-(β-<SCP>d</SCP>-ribofuranosyl)-vic-triazolo[4,5-b]pyridin-5-one Derivatives

Author

Wang, P., Du, J., Rachakonda, S., Chun, B.-K., Tharnish, P. M., Stuyver, L. J., Otto, M. J., Schinazi, R. F., and Watanabe, K. A.

Abstract

Several 6- and 7-monosubstituted N 3,5‘-cyclo-4-(β-d-ribofuranosyl)-vic-triazolo[4,5-b]pyridin-5-one derivatives as well as the 5-thiono analogue were synthesized, providing structure−anti-hepatitis C virus (HCV) activity relationships for the series. Among the compounds synthesized, the 6-bromo, 7-methylamino, and 5-thiono analogues exhibited more potent anti-HCV activity in an HCV subgenomic replicon cell based assay (EC90 = 1.9, 7.4, and 10.0 μM, respectively) than the lead compound N 3,5‘-cyclo-4-(β-d-ribofuranosyl)-vic-triazolo[4,5-b]pyridin-5-one (EC90 = 79.8 μM).

Published
2005

38. Design, Synthesis, and Antiviral Activity of 2‘-Deoxy-2‘-fluoro-2‘-C-methylcytidine, a Potent Inhibitor of Hepatitis C Virus Replication

Author

Clark, J. L., Hollecker, L., Mason, J. C., Stuyver, L. J., Tharnish, P. M., Lostia, S., McBrayer, T. R., Schinazi, R. F., Watanabe, K. A., Otto, M. J., Furman, P. A., Stec, W. J., Patterson, S. E., and Pankiewicz, K. W.

Abstract

The pyrimidine nucleoside beta-d-2‘-deoxy-2‘-fluoro-2‘-C-methylcytidine (1) was designed as a hepatitis C virus RNA-dependent RNA polymerase (HCV RdRp) inhibitor. The title compound was obtained by a DAST fluorination of N4-benzoyl-1-(2-methyl-3,5-di-O-benzoyl-β-d-arabinofuranosyl]cytosine (6) to provide N4-benzoyl-1-[2-fluoro-2-methyl-3,5-di-O-benzoyl-β-d-ribofuranosyl]cytosine (7a). The protected 2‘-C-methylcytidine (7c) was obtained as a byproduct from the DAST fluorination and allowed for the preparation of two biologically active compounds from a common precursor. Compound 1 and 2‘-C-methylcytidine were assayed in a subgenomic HCV replicon assay system and found to be potent and selective inhibitors of HCV replication. Compound 1 shows increased inhibitory activity in the HCV replicon assay compared to 2‘-C-methylcytidine and low cellular toxicity.

Published
2005

39. Synthesis of N<SUP>3</SUP>,5‘-Cyclo-4-(β-<SCP>d</SCP>-ribofuranosyl)-vic-triazolo[4,5-b]pyridin-5-one, a Novel Compound with Anti-Hepatitis C Virus Activity

Author

Wang, P., Hollecker, L., Pankiewicz, K. W., Patterson, S. E., Whitaker, T., McBrayer, T. R., Tharnish, P. M., Sidwell, R. W., Stuyver, L. J., Otto, M. J., Schinazi, R. F., and Watanabe, K. A.

Abstract

A novel anti-hepatitis C virus (HCV) agent, N3,5‘-cyclo-4-(β-d-ribofuranosyl)-vic-triazolo[4,5-b]pyridinin-5-one, was identified, and the structure was confirmed by chemical synthesis from 2-hydroxy-5-nitropyridine.

Published
2004

40. Hepatitis virus infections in heart transplant recipients: Epidemiology, natural history, characteristics, and impact on survival

Author

Lunel, F., Cadranel, J.F., Rosenheim, M., Dorent, R., Di-Martino, V., Payan, C., Fretz, C., Ghoussoub, J.J., Bernard, B., Dumont, B., Perrin, M., Gandjbachkh, I., Ruraux, J.M., Stuyver, L., and Opolon, P.

Abstract

Background & Aims: We have observed a high prevalence of hepatitis B virus (HBV) and hepatitis C virus (HCV) infection in heart transplant recipients (HTRs). The aim of this study was to assess the epidemiology, natural history, and clinical and biological characteristics of viral hepatitis in HTRs. Methods: From 1983 to 1992, 874 patients underwent heart transplantation at the Pitie-Salpetriere Hospital, Paris, France, 459 of whom qualified for analysis. A total of 140 patients had post-transplantation hepatitis B, C, or non-A-E. Sixty-nine patients developed HBV infection, 49 HCV infection, 11 HBV-HCV coinfection, and 11 non-A-E hepatitis. Results: HBV was transmitted nosocomially from patient to patient, most likely during endomyocardial biopsies. HCV was mainly transmitted through blood transfusions or the transplanted organ. Clinical and biological findings after 2 years of follow-up showed that 3 patients with an HBV genotype A precore mutant had severe or subfulminant hepatitis and that patients with HBV and HCV infection always progressed to chronicity. In general, patients had mild alanine aminotransferase level increases, a high level of viral replication, and few severe histologic lesions, except for patients infected by precore HBV mutants. Patients coinfected by HBV and HCV tended to have more severe liver lesions. The survival rate 5 years after transplantation in patients with viral hepatitis (HBV, 81%; HCV, 89%; HBV and HCV coinfection, 100%; non-A-E hepatitis, 73%) was similar to that in patients without liver test abnormalities (76%). The actuarial survival curve was also similar in patients with or without liver test abnormalities. Conclusions: In our experience, histologic liver lesions do not progress rapidly in patients with post-heart transplant infection caused by HBV or HCV. HBV or HCV infection seems to have little impact on the 5-year survival rate of HTRs.

Published
2000
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46. A compact device for digital droplet PCR

Author

Wiederkehr, R. S., Jones, B., Majeed, B., Colle, F., Chen, W. -C, Tim Stakenborg, Fiorini, P., Lagae, L., Schmidt, K., Stuyver, L., and Jacobson, Stephen

Abstract

In this work, the fabrication and testing of a miniaturized device to perform all steps necessary for digital droplet polymerase chain reaction (ddPCR) within a single chip is presented. The microfluidic chip, made in silicon, contains a T-junction for droplet generation along with a microreactor for temperature cycling. The temperature is controlled by means of an external, miniaturized thermoelectric element. The number of fluorescent droplets after PCR amplification is determined using a fluorescent microscope; furthermore, individual droplet fluorescence is recorded at each cycle, thus enabling real time PCR analysis. The microreactor accommodates about 2500-3000 droplets of uniform volume varying in the 55-65 pL range, allowing the direct and accurate detection of human genomic DNA in concentrations from 0.06 to 40 ng/μL. ispartof: pages:1000-1002 ispartof: Proceedings of the 18th International Conference on Miniaturized Systems for Chemistry and Life Science pages:1000-1002 ispartof: International Conference on Miniaturized Systems for Chemistry and Life Science (Microtas 2014) location:San Antonio, TX USA date:26 Oct - 31 Oct 2014 status: published

48. HCV infection according to HIV status in Brazzaville, Congo

Author

Fretz, C., Tuppin, P., Stuyver, L., Delamare, O., Samba-Lefevres, M.C., Gueguen, M., Fournel, J.J., and Jeannel, D.

Subjects
Hepatitis C virus -- Diagnosis, HIV infection -- Complications, Congo (Brazzaville) -- Health aspects
Abstract

According to an abstract submitted by the authors to the 3rd International Meeting on Hepatitis C Virus and Related Viruses, held August 30 - September 3, 1995, in Gold Coast, [...]

Published
1995

49. A comparative analysis of HIV drug resistance interpretation based on short reverse transcriptase sequences versus full sequences

Author

Stevens Wendy, Wallis Carole L, Van der Borght Koen, Winters Bart, Van Craenenbroeck Elke, Bronze Michelle, Steegen Kim, Rinke de Wit Tobias F, and Stuyver Lieven J

Subjects
Immunologic diseases. Allergy, RC581-607
Abstract

Abstract Background As second-line antiretroviral treatment (ART) becomes more accessible in resource-limited settings (RLS), the need for more affordable monitoring tools such as point-of-care viral load assays and simplified genotypic HIV drug resistance (HIVDR) tests increases substantially. The prohibitive expenses of genotypic HIVDR assays could partly be addressed by focusing on a smaller region of the HIV reverse transcriptase gene (RT) that encompasses the majority of HIVDR mutations for people on ART in RLS. In this study, an in silico analysis of 125,329 RT sequences was performed to investigate the effect of submitting short RT sequences (codon 41 to 238) to the commonly used virco®TYPE and Stanford genotype interpretation tools. Results Pair-wise comparisons between full-length and short RT sequences were performed. Additionally, a non-inferiority approach with a concordance limit of 95% and two-sided 95% confidence intervals was used to demonstrate concordance between HIVDR calls based on full-length and short RT sequences. The results of this analysis showed that HIVDR interpretations based on full-length versus short RT sequences, using the Stanford algorithms, had concordance significantly above 95%. When using the virco®TYPE algorithm, similar concordance was demonstrated (>95%), but some differences were observed for d4T, AZT and TDF, where predictions were affected in more than 5% of the sequences. Most differences in interpretation, however, were due to shifts from fully susceptible to reduced susceptibility (d4T) or from reduced response to minimal response (AZT, TDF) or vice versa, as compared to the predicted full RT sequence. The virco®TYPE prediction uses many more mutations outside the RT 41-238 amino acid domain, which significantly contribute to the HIVDR prediction for these 3 antiretroviral agents. Conclusions This study illustrates the acceptability of using a shortened RT sequences (codon 41-238) to obtain reliable genotype interpretations by virco®TYPE and Stanford algorithms. Implementation of this simplified protocol could significantly reduce the cost of both resistance testing and ARV treatment monitoring in RLS.

Published
2010
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50. HIV-1 V3 envelope deep sequencing for clinical plasma specimens failing in phenotypic tropism assays

Author

Florence Eric, De Wit Stephane, Kabeya Kabamba, Vaira Dolores, Fransen Katrien, Van Baelen Kurt, Thys Kim, Rondelez Evelien, Van Eygen Veerle, Mostmans Wendy, Van Marck Herwig, Vandenbroucke Ina, Moutschen Michel, Vandekerckhove Linos, Verhofstede Chris, and Stuyver Lieven J

Subjects
Immunologic diseases. Allergy, RC581-607
Abstract

Abstract Background HIV-1 infected patients for whom standard gp160 phenotypic tropism testing failed are currently excluded from co-receptor antagonist treatment. To provide patients with maximal treatment options, massively parallel sequencing of the envelope V3 domain, in combination with tropism prediction tools, was evaluated as an alternative tropism determination strategy. Plasma samples from twelve HIV-1 infected individuals with failing phenotyping results were available. The samples were submitted to massive parallel sequencing and to confirmatory recombinant phenotyping using a fraction of the gp120 domain. Results A cut-off for sequence reads interpretation of 5 to10 times the sequencing error rate (0.2%) was implemented. On average, each sample contained 7 different V3 haplotypes. V3 haplotypes were submitted to tropism prediction algorithms, and 4/14 samples returned with presence of a dual/mixed (D/M) tropic virus, respectively at 3%, 10%, 11%, and 95% of the viral quasispecies. V3 tropism prediction was confirmed by gp120 phenotyping, except for two out of 4 D/M predicted viruses (with 3 and 95%) which were phenotypically R5-tropic. In the first case, the result was discordant due to the limit of detection for the phenotyping technology, while in the latter case the prediction algorithms were not computing the viral tropism correctly. Conclusions Although only demonstrated on a limited set of samples, the potential of the combined use of "deep sequencing + prediction algorithms" in cases where routine gp160 phenotype testing cannot be employed was illustrated. While good concordance was observed between gp120 phenotyping and prediction of R5-tropic virus, the results suggest that accurate prediction of X4-tropic virus would require further algorithm development.

Published
2010
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